RETRACTED: NFKB1 mediates Th1/Th17 activation in the pathogenesis of psoriasis

Zhou, Fusheng; Zhu, Zhengwei; Gao, Jinping; Yang, Chao; Wen, Leilei; Liu, Lu; Zuo, Xianbo; Zheng, Xiaodong; Shi, Yinjuan; Zhu, Caihong; Liang, Bo; Yin, Xianyong; Wang, Wenjun; Cheng, Hui; Shen, Songke; Tang, Xianfa; Tang, Huayang; Sun, Liangdan; Zhang, Anping; Yang, Sen; Zhang, Xuejun; Sheng, Yujun

doi:10.1016/j.cellimm.2018.04.016

Cited by 32 publications

(25 citation statements)

References 24 publications

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“…Moreover, as it is well known that psoriasis is an inflammatory disease mediated by T lymphocytes, abnormal differentiation of T lymphocytes (especially 1 and 17 cells) and excessive secretion of proinflammatory factors (such as ILs) are closely related to the progression of the disease [59]. In this study, we have also demonstrated that there are diverse critical signaling pathways related to T lymphocytes differentiation and proinflammatory factors production (TLRs, JAK-STAT, and NF-κB) regulated by QBF on psoriasis therapy [60][61][62].…”

Section: Discussionsupporting

confidence: 55%

Investigation on the Mechanism of Qubi Formula in Treating Psoriasis Based on Network Pharmacology

Zhou

Zhang²,

Tao

2020

Evidence-Based Complementary and Alternative Medicine

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Objective. To elucidate the pharmacological mechanisms of Qubi Formula (QBF), a traditional Chinese medicine (TCM) formula which has been demonstrated as an effective therapy for psoriasis in China. Methods. The Traditional Chinese Medicine Systems Pharmacology (TCMSP) database, BATMAN-TCM database, and literature search were used to excavate the pharmacologically active ingredients of QBF and to predict the potential targets. Psoriasis-related targets were obtained from Therapeutic Target Database (TTD), DrugBank database (DBD), MalaCards database, and DisGeNET database. Then, we established the network concerning the interactions of potential targets of QBF with well-known psoriasis-related targets by using protein-protein interaction (PPI) data in String database. Afterwards, topological parameters (including DNMC, Degree, Closeness, and Betweenness) were calculated to excavate the core targets of Qubi Formula in treating psoriasis (main targets in the PPI network). Cytoscape was used to construct the ingredients-targets core network for Qubi Formula in treating psoriasis, and ClueGO was used to perform GO-BP and KEGG pathway enrichment analysis on these core targets. Results. The ingredient-target-disease core network of QBF in treating psoriasis was screened to contain 175 active ingredients, which corresponded to 27 core targets. Additionally, enrichment analysis suggested that targets of QBF in treating psoriasis were mainly clustered into multiple biological processes (associated with nuclear translocation of proteins, cellular response to multiple stimuli (immunoinflammatory factors, oxidative stress, and nutrient substance), lymphocyte activation, regulation of cyclase activity, cell-cell adhesion, and cell death) and related pathways (VEGF, JAK-STAT, TLRs, NF-κB, and lymphocyte differentiation-related pathways), indicating the underlying mechanisms of QBF on psoriasis. Conclusion. In this work, we have successfully illuminated that Qubi Formula could relieve a wide variety of pathological factors (such as inflammatory infiltration and abnormal angiogenesis) of psoriasis in a “multicompound, multitarget, and multipathway” manner by using network pharmacology. Moreover, our present outcomes might shed light on the further clinical application of QBF on psoriasis treatment.

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Section: Discussionsupporting

confidence: 55%

Investigation on the Mechanism of Qubi Formula in Treating Psoriasis Based on Network Pharmacology

Zhou

Zhang²,

Tao

2020

Evidence-Based Complementary and Alternative Medicine

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“…Our results show that ozone treatment can significantly inhibit IMQ-induced increases in the number and active function of Th17 cells. Activation of the NF-κB signaling pathway can induce the activation of Th17 cells [52]. Therefore, ozone-mediated suppression of the activation of Th17 cells is probably due to the inhibition of NF-κB pathways.…”

Section: Discussionmentioning

confidence: 99%

Ozone Therapy Attenuates NF-κB-Mediated Local Inflammatory Response and Activation of Th17 Cells in Treatment for Psoriasis

Zeng

et al. 2020

Int. J. Biol. Sci.

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Ozone therapy has been widely used to treat many skin diseases, including infections, allergic dermatosis, and skin ulcers. However, its efficacy as a treatment for psoriasis is unclear. In this study, we explored the clinical efficacy and the underlying molecular mechanisms of ozone therapy on psoriasis. We found that topical ozone treatment significantly decreased patients' psoriasis area and severity index (PASI) scores and the expression of psoriasis-associated cytokines in their peripheral blood CD4 + T cells. In the IMQ-induced psoriasis mouse model, topical ozone treatment significantly inhibited the formation of IMQ-induced psoriasis-like lesions and the expression of psoriasis-associated inflammatory factors. High-throughput sequencing confirmed that IMQ-induced activation of toll-like receptor 2 (TLR2)/ nuclear factor-κB (NF-κB) signaling pathway was significantly suppressed in psoriasis-like lesions after topical ozone treatment. Furthermore, the activation of spleen T helper (Th) 17 cells was blocked in the mouse model; this was associated with the downregulation of cytokines and NF-κB pathways upon topical ozone treatment. Ozone therapy can attenuate local inflammatory reactions and the activation of Th17 cells in psoriasis by inhibiting the NF-κB pathway. Our results show that ozone therapy is effective in treating psoriasis. We recommend further evaluations for its clinical applications.

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“…[18] Moreover, NFKB1 from this module mediates Th1/Th17 activation in the pathogenesis of psoriasis and probably other autoimmune diseases. [19] Green genes also had more DMRs, either in the gene bodies or in GH elements mapped to the genes, suggesting that TNFa stimulation causes more long-lasting changes to gene expression to genes in the green set than to other sets.…”

Section: Plos Onementioning

confidence: 99%

Global expression and CpG methylation analysis of primary endothelial cells before and after TNFa stimulation reveals gene modules enriched in inflammatory and infectious diseases and associated DMRs

et al. 2020

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Endothelial cells are a primary site of leukocyte recruitment during inflammation. An increase in tumor necrosis factor-alpha (TNFa) levels as a result of infection or some autoimmune diseases can trigger this process. Several autoimmune diseases are now treated with TNFa inhibitors. However, genomic alterations that occur as a result of TNF-mediated inflammation are not well understood. To investigate molecular targets and networks resulting from increased TNFa, we measured DNA methylation and gene expression in 40 human umbilical vein endothelial cell primary cell lines before and 24 hours after stimulation with TNFa via microarray. Weighted gene co-expression network analysis identified 15 gene groups (modules) with similar expression correlation patterns; four modules showed a strong association with TNFa treatment. Genes in the top TNFa-associated module were all up-regulated, had the highest proportion of hypomethylated regions, and were associated with 136 Disease Ontology terms, including autoimmune/inflammatory, infectious and cardiovascular diseases, and cancers. They included chemokines CXCL1, CXCL10 and CXCL8, and genes associated with autoimmune diseases including HLA-C, DDX58, IL4, NFKBIA and TNFAIP3. Cardiovascular and metabolic disease genes, including APOC1, ACLY, ELOVL6, FASN and SCD, were overrepresented in a module that was not associated with TNFa treatment. Of 223 hypomethylated regions identified, several were in promoters of autoimmune disease GWAS loci (ARID5B, CD69, HDAC9, IL7R, TNIP1 and TRAF1). Results reveal specific gene groups acting in concert in endothelial cells, delineate those driven by TNFa, and establish their relationship to DNA methylation changes, which has strong implications for understanding disease etiology and precision medicine approaches.

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RETRACTED: NFKB1 mediates Th1/Th17 activation in the pathogenesis of psoriasis

Cited by 32 publications

References 24 publications

Investigation on the Mechanism of Qubi Formula in Treating Psoriasis Based on Network Pharmacology

Investigation on the Mechanism of Qubi Formula in Treating Psoriasis Based on Network Pharmacology

Ozone Therapy Attenuates NF-κB-Mediated Local Inflammatory Response and Activation of Th17 Cells in Treatment for Psoriasis

Global expression and CpG methylation analysis of primary endothelial cells before and after TNFa stimulation reveals gene modules enriched in inflammatory and infectious diseases and associated DMRs

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